In what may become the most far-reaching effects of the failed Vytorin trial, experts are questioning the sacred link between cholesterol and heart disease. After all, Vytorin did do a better job of lowering LDL in the Enhance trial. So why did it utterly fail at holding off atherosclerosis? Why did Pfizer's experimental torcetrapib lower "bad" cholesterol and raise "good" cholesterol--and yet cause heart attacks and strokes, rather than prevent them? Why did AstraZeneca's Crestor fail to beat placebo at preventing heart attacks in the Corona study released last fall?
The ramifications of these questions are huge. The "lower LDL is good" is such a core belief in cardiology that drug makers have only had to prove that their meds lower the offending substance--not that the products actually prevented heart attack or stroke--to get FDA approval. And pharma sells billions of dollars worth of cholesterol-lowering drugs every year. If the link between LDL and disease were to be severed, or even weakened, companies would suffer.
Now, a couple of statins--namely Lipitor and Zocor--have proven to reduce heart attacks and strokes in post-marketing trials. But is it the LDL-lowering itself that cut the risk? Or some other unknown action of those drugs?
Outcomes trials of Zetia, the med added to Zocor to make Vytorin, and Vytorin itself are ongoing. Tuesday, the American Heart Association called for the Zetia events trial to be finished as quickly as possible. But in another bit of Enhance fallout, patients in at least one of the outcomes trials have panicking, calling up clinical investigators to ask whether they should stay in the study.
- see this analysis from the New York Times
- read about trial patients' panic and other statin issues in USA Today
- get BusinessWeek's take on the efficacy of cholesterol meds